안정준 (충남대)

김형민 (충남대학교)

안정준 (충남대)

김형민 (충남대학교)

The extensive application of organophosphate flame retardants (OPFRs) in a wide range of consumer products has resulted in escalating environmental contamination. OPFRs have been consistently detected in aquatic and terrestrial ecosystems, with recent findings also reporting their presence in food sources. The pervasive distribution of these compounds highlights the urgency for a thorough investigation into the molecular mechanisms underlying their biological effects. Human exposure predominantly occurs through ingestion of contaminated water and food, placing the gastrointestinal tract—particularly the intestinal epithelium—as a primary site of interaction. The intestinal epithelial barrier plays a critical role as the first line of defense against ingested toxicants. Prior research has demonstrated that OPFRs can provoke intestinal inflammation, emphasizing their potential to disrupt gut homeostasis. In the present study, a combination of LC-MS–based metabolomic and transcriptomic analyses was applied to biological models exposed to OPFRs, which are known to induce oxidative stress. Comparative profiling revealed pronounced alterations in metabolite levels between control and OPFR-treated groups. These differential metabolites were enriched in oxidative stress–related metabolic pathways, including purine metabolism and pantothenate and CoA biosynthesis. Overall, the findings provide mechanistic insights into the toxicological effects of OPFRs and reveal conserved molecular responses in both human colon epithelial cells (Caco-2) and Caenorhabditis elegans (C. elegans) following exposure. This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korean government (MSIT) (Grant No. 2022R1A5A7085156).​